PATTERNS OF MUSCLE SPINDLE AFFERENT STIMULATION BY ALKYLAMMONIUM COMPOUNDS

¹ Department of Pharmacology, University of illinois College of Medicine, Chicago, Illinois

Activities of triceps surac muscle spindle afferents isolated from dorsal root filaments were recorded in spinal cats. The acceleration of discharge frequency of group Ia and group II spindle afferent fibers produced by i.a. administration of succinylcholine, acetylcholine, tetramethylammonium, nicotine and decamethonium was studied. The magnitude of the afferent activation produced by these compounds, with the exception of acetylcholine and decamethonium, was a positive function of the conduction velocity of the afferent fiber; thus, relatively selective activation of group Ia fibers could be achieved. Acetylcholine and decamethonium induced an increase in afferent activity in all fibers, the magnitude of which was not related to conduction velocity of the afferent fibers. Tetraethylammonium, pentamethonium and hexamethonium were inactive in altering spindle afferent activity in doses up to 8 mg. After complete block of neuromuscular transmission in extra- and intrafusal muscle fibers by tubocurarine, the spindle afferent activation by acetylcholine and decamethonium was almost or completely abolished, whereas that produced by succinylcholine, nicotine or tetramethylammonium was depreesed by approximately 50%. It is postulated that each of the various cholinergic agents has a spectrum of actions on muscle spindle systems. Specifically, these experiments could be interpreted to indicate that all of the cholinergic agents act at the neuromuscular junctions of the intrafusal muscle fibers. Under this premise, succinyicholine and nicotine could be interpreted to activate the contracture-like components of the intrafusal fibers regulating spindle dynamic sensitivity to a greater extent than does acetylcholine or decamethonium. It is suggested that acetylcholine and decamethonium could have actions presynaptically at the fusimotor nerve terminals in addition to their postsynaptic effects.